Circ_0084188通过调控miR-654-3p和kruppel-like factor 12促进结直肠癌进展。

IF 2.7 4区 医学 Q3 MEDICINE, RESEARCH & EXPERIMENTAL
Kaohsiung Journal of Medical Sciences Pub Date : 2023-11-01 Epub Date: 2023-09-12 DOI:10.1002/kjm2.12749
Cui-Cui Wu, Bai-Chun Hou, Yu-Han Yang, Xue-Feng Li, Hong-Chao Ma, Bin-Xian Li
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引用次数: 0

摘要

探讨circ_0084188在癌症(CRC)中的生物学作用及其机制。实时定量聚合酶链式反应和蛋白质印迹法分别检测CRC细胞系(HCT116和SW480)中的RNA水平和蛋白质水平。通过细胞计数试剂盒-8测定法、5-乙炔基-2'-脱氧尿苷测定法和集落形成测定法评估细胞增殖。使用流式细胞术测定细胞凋亡。通过transwell法测定细胞迁移和侵袭。球体形成效率通过球体形成测定法测定。microRNA-654-3p(miR-654-3p)与circ_0084188或Kruppel样因子12(KLF12)之间的相互作用通过双荧光素酶报告子、RNA免疫沉淀和RNA下拉测定得到证实。利用CRC小鼠模型中的异种移植来探索circ_0084188在体内的作用。Circ_0084188在CRC组织和细胞中过表达。Circ_0084488沉默抑制CRC细胞的增殖、迁移、侵袭和干性,并诱导细胞凋亡。Circ_00084188充当miR-654-3p的海绵,Circ_0084188通过海绵miR-654-3p调节CRC细胞行为。此外,KLF12是miR-654-3p的靶点,miR-654-3p-过表达通过下调KLF12抑制CRC细胞的恶性行为。在机制上,circ_0084188吸收miR-654-3p以调节CRC细胞中KLF12的表达。此外,circ_0084188下调抑制了体内肿瘤生长。Circ-0084188敲低可能通过调节miR-654-3p/KLF12轴部分抑制CRC进展,为CRC的发病机制提供了新的见解。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Circ_0084188 promotes colorectal cancer progression by sponging miR-654-3p and regulating kruppel-like factor 12.

To investigate the biological role and mechanism of circ_0084188 in colorectal cancer (CRC). Real-time quantitative polymerase chain reaction and western blot assay were used to detect RNA levels and protein levels in CRC cell lines (HCT116 and SW480), respectively. Cell proliferation was evaluated by Cell Counting Kit-8 assay, 5-ethynyl-2'-deoxyuridine assay, and colony formation assays. Cell apoptosis was determined using flow cytometry. Cell migration and invasion were measured by transwell assay. Sphere formation efficiency was determined by sphere formation assay. The interaction between microRNA-654-3p (miR-654-3p) and circ_0084188 or Kruppel-like factor 12 (KLF12) was confirmed by a dual-luciferase reporter, RNA immunoprecipitation and RNA pull-down assays. Xenograft in CRC mice model was utilized for exploring the role of circ_0084188 in vivo.Circ_0084188 was overexpressed in CRC tissues and cells. Circ_0084188 silencing suppressed cell proliferation, migration, invasion, and stemness and induced apoptosis in CRC cells. Circ_0084188 acted as a sponge for miR-654-3p, and circ_0084188 regulated CRC cell behaviors via sponging miR-654-3p. Moreover, KLF12 was a target of miR-654-3p, and miR-654-3p overexpression inhibited the malignant behaviors of CRC cells by downregulating KLF12. Mechanically, circ_0084188 sponged miR-654-3p to regulate KLF12 expression in CRC cells. In addition, circ_0084188 downregulation inhibited tumor growth in vivo.Circ_0084188 knockdown might repress CRC progression partially via regulating the miR-654-3p/KLF12 axis, providing a novel insight into the pathogenesis of CRC.

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来源期刊
Kaohsiung Journal of Medical Sciences
Kaohsiung Journal of Medical Sciences 医学-医学:研究与实验
CiteScore
5.60
自引率
3.00%
发文量
139
审稿时长
4-8 weeks
期刊介绍: Kaohsiung Journal of Medical Sciences (KJMS), is the official peer-reviewed open access publication of Kaohsiung Medical University, Taiwan. The journal was launched in 1985 to promote clinical and scientific research in the medical sciences in Taiwan, and to disseminate this research to the international community. It is published monthly by Wiley. KJMS aims to publish original research and review papers in all fields of medicine and related disciplines that are of topical interest to the medical profession. Authors are welcome to submit Perspectives, reviews, original articles, short communications, Correspondence and letters to the editor for consideration.
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